Allele Dmel\zip^{FL.Scer\UAS.T:Avic\GFP}

General Information
Symbol	Dmel\zip^{FL.Scer\UAS.T:Avic\GFP}	Species	D. melanogaster
Name		FlyBase ID	FBal0190596
Feature type	allele	Associated gene	Dmel\zip

Allele class
Mutagen	in vitro construct - coding region fusion, in vitro construct - regulatory fusion
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	in vitro construct - coding region fusion (Franke et al., 2005) in vitro construct - regulatory fusion (Franke et al., 2005)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference Construct: Scer\UAS sequences drive expression of full-length zip, tagged with T:Avic\GFP at the N terminus. (Franke et al., 2005)
Carried in construct	P{UAS-zip.GFP.FL} (Franke et al., 2005, Franke et al., 2006, Rodriguez-Diaz et al., 2008, Bertet et al., 2009, Monier et al., 2010, Hatan et al., 2011, Martin et al., 2009, Franke et al., 2010, Franke et al., 2007)
Tagged with	T:Avic\GFP (Franke et al., 2005)
Cytology
Phenotypic Data
Phenotypic Class
	visible, with Scer\GAL4^en-e16E (Franke et al., 2010) visible, with Scer\GAL4^en-e16E, zip¹ (Franke et al., 2010)
Phenotype Manifest In
	embryonic dorsal epidermis, with Scer\GAL4^en-e16E (Franke et al., 2005) embryonic dorsal epidermis, with Scer\GAL4^en-e16E, zip²/zip¹ (Franke et al., 2005) wing vein \| ectopic, with Scer\GAL4^en-e16E (Franke et al., 2010) wing vein \| ectopic, with Scer\GAL4^en-e16E, zip¹ (Franke et al., 2010)
Detailed Description
	Statement Reference Expression of a single copy of zip[FL.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[en-e16E] results in a wing vein expansion phenotype in 82% of wings. The penetrance of this phenotype is slightly decreased (to 72%) in a zip[1]/+ background. (Franke et al., 2010) Expression of zip[FL.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[arm.T:Hsim\VP16] results in the loss of para-segmental boundary straightness. (Monier et al., 2010) Embryos expressing zip[FL.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[mat.αTub67C.T:Hsim\VP16] do not show germ-band extension defects, and no change is observed in apical cell surface size. (Bertet et al., 2009) In transgenic mosaic embryos in which some cells express zip^{FL.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^e22c in a zip¹/zip² background, leading-edge cells that do not express zip^{FL.Scer\UAS.T:Avic\GFP} cannot maintain tension and are stretched by neighbouring zip^{FL.Scer\UAS.T:Avic\GFP} expressing cells. The length of contiguous regions of Scer\GAL4^e22c>zip^{FL.Scer\UAS.T:Avic\GFP} expressing leading-edge cells along the supracellular purse string decrease in length over time, indicative of contraction. In contrast, non zip^{FL.Scer\UAS.T:Avic\GFP}-expressing contiguous regions fail to contract, increasing in length over time. In transgenic mosaic embryos in which some cells express zip^{FL.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^sqh.PW in a zip¹/zip² background, Scer\GAL4^sqh.PW>zip^{FL.Scer\UAS.T:Avic\GFP} expressing leading-edge cells that contact Scer\GAL4^sqh.PW>zip^{FL.Scer\UAS.T:Avic\GFP} expressing amnioserosa cells are severely contracted, and the scalloped morphology of the early leading edge is enhanced. In contrast, when non-expressing leading-edge cells contact non-expressing amnioserosa cells the leading edge cells fail to contract and become stretched. When non-expressing leading-edge cells contact Scer\GAL4^sqh.PW>zip^{FL.Scer\UAS.T:Avic\GFP}-expressing amnioserosa cells, leading-edge cells show some contraction. Finally, Scer\GAL4^sqh.PW>zip^{FL.Scer\UAS.T:Avic\GFP}-expressing cells show some contraction when they contact non-expressing amnioserosa cells, although this is to a lesser extent than when both cell types express zip^{FL.Scer\UAS.T:Avic\GFP}. Nonexpressing leading-edge cells fail to incorporate into the canthus and cause inward progression of the canthus to stall. These nonexpressors never get fully incorporated into the seam - instead, a small gap is formed when zipping fails and closure bypasses the nonexpressing cells to initiate a new seam. In contrast, Scer\GAL4^sqh.PW>zip^{FL.Scer\UAS.T:Avic\GFP}-expressing cells are incorporated into each canthus at a similar and nearly constant rate. In transgenic mosaic embryos in which some amnioserosa cells express zip^{FL.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^c381 in a zip¹/zip² background, nonexpressing amnioserosa cells fail to contract apically and remain rounded. These cells do show an apical shape change at later stages but this may be due to forces generated by surrounding Scer\GAL4^c381>zip^{FL.Scer\UAS.T:Avic\GFP}-expressing amnioserosa cells and the approaching lateral-epidermis sheet. Embryos that express zip^{FL.Scer\UAS.T:Avic\GFP} under the control of Scer\GAL4^en-e16E in a zip¹/zip² background display stripe-alignment defects in 65% of cases. (Franke et al., 2005)
External Data
Linkouts
Interactions
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference
Xenogenetic Interactions
Statement Reference Ubiquitous overexpression of zip^{FL.Scer\UAS.T:Avic\GFP}, under the control of the Scer\GAL4^sqh.PW, rescues dorsal closure in more than 84% of zip¹/zip²; Dpse\l(2)gl^+t12.2/Dpse\l(2)gl^+t12.2 embryos. 61% of these rescued flies survive to hatch as larvae, 41% survive to pupal stages and 2.8% eclose as adults. Expression of zip^{FL.Scer\UAS.T:Avic\GFP} in the epidermis and a few amnioserosa cells, driven by Scer\GAL4^e22c, rescues the zip¹/zip²; Dpse\l(2)gl^+t12.2/Dpse\l(2)gl^+t12.2 dorsal closure phenotype in 88% of embryos. Rescued flies survive to larval stages in 60% of cases and to pupal stages in 21% of cases, although no flies eclose. Expression of zip^{FL.Scer\UAS.T:Avic\GFP} in the amnioserosa, driven by Scer\GAL4^c381, rescues the dorsal closure phenotype of Dpse\l(2)gl^+t12.2/Dpse\l(2)gl^+t12.2 mutants in 82% of embryos. However, none of the rescued embryos survive to larval stages. Similarly, when zip^{FL.Scer\UAS.T:Avic\GFP} expression is driven in the leading edge by Scer\GAL4^LE, dorsal closure is rescued in 87% of embryos, but only 1% of flies survive to larval stages. zip^{FL.Scer\UAS.T:Avic\GFP} expression in epidermal stripes, driven by Scer\GAL4^en-e16E, rescues dorsal closure in only half of embryos and does not rescue lethality. (Franke et al., 2005)
Complementation & Rescue Data
Partially rescues	Scer\GAL4^sqh.PW/zip^{FL.Scer\UAS.T:Avic\GFP} partially rescues zip²/zip¹ (Franke et al., 2010, Franke et al., 2007)
Comments	Expression of zip[FL.Scer\UAS.T:Avic\GFP] under the control of Scer\GAL4[sqh.PW] rescues the embryonic lethality of zip[1]/zip[2] animals. 86 +/- 2% of the rescued animals survive to the pupal stage, but only 6 +/- 7% eclose as adults. (Franke et al., 2007)
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 1 )
Reported As
Symbol Synonym	zip^{FL.Scer\UAS.T:Avic\GFP}
Name Synonym
Secondary FlyBase IDs

References ( 9 )
Research paper	Hatan et al., 2011, J. Cell Biol. 192(2): 307--319 The Drosophila blood brain barrier is maintained by GPCR-dependent dynamic actin structures. [FBrf0212807] Franke et al., 2010, Dev. Biol. 345(2): 117--132 Nonmuscle myosin II is required for cell proliferation, cell sheet adhesion and wing hair morphology during wing morphogenesis. [FBrf0211576] Monier et al., 2010, Nat. Cell Biol. 12(1): 60--65 An actomyosin-based barrier inhibits cell mixing at compartmental boundaries in Drosophila embryos. [FBrf0209576] Bertet et al., 2009, Development 136(24): 4199--4212 Repression of Wasp by JAK/STAT signalling inhibits medial actomyosin network assembly and apical cell constriction in intercalating epithelial cells. [FBrf0209348] Martin et al., 2009, Nature 457(7228): 495--499 Pulsed contractions of an actin-myosin network drive apical constriction. [FBrf0206985] Rodriguez-Diaz et al., 2008, HFSP J. 2(4): 220--237 Actomyosin purse strings: renewable resources that make morphogenesis robust and resilient. [FBrf0207810] Franke et al., 2007, Hum. Mol. Genet. 16(24): 3160--3173 An MYH9 human disease model in flies: site-directed mutagenesis of the Drosophila non-muscle myosin II results in hypomorphic alleles with dominant character. [FBrf0201204] Franke et al., 2006, Cell Motility Cytoskel. 63(10): 604--622 Native nonmuscle myosin II stability and light chain binding in Drosophila melanogaster. [FBrf0193420] Franke et al., 2005, Curr. Biol. 15(24): 2208--2221 Nonmuscle myosin II generates forces that transmit tension and drive contraction in multiple tissues during dorsal closure. [FBrf0190012]

Allele Dmel\zipFL.Scer\UAS.T:Avic\GFP

Allele Dmel\zip^{FL.Scer\UAS.T:Avic\GFP}